Mixed viral infections in plants are very common in nature, and occur when two or more viruses are able to infect the same host. The interactions between the different viruses in mixed infections can be synergistic or antagonistic, depending on whether the outcome is positive or negative. Except in some complex diseases caused by severe synergistic interactions, often mixed infections remain unnoticed and their impact on vector transmission of viruses by insects is largely unknown. The main objective of this work was to evaluate the biological effects of mixed virus infections in plants. Mixed infections caused by Cucurbit yellow stunting disorder virus (CYSDV) and Watermelon mosaic virus (WMV) has been studied, paying special attention to the interaction between them, how it affects the host plant, and the possible impact on vector transmission. Also, the possible influence of mixed infections on intrinsic biological aspects of the viruses has been evaluated, as in the case of the polymerase slippage mechanism that allows the expression of additional gene products in viruses of the family Potyviridae, such as the ipomovirus Coccinia mottle virus (CocMoV), which in addition to the usual motive resulting in expression of P3N-PIPO, it contains a similar motif in P1a, from which new products named P1aN-SOG (from "Short Out-of-frame Gene-product ") and P1aNALT could originate. Our work shows the accumulation dynamics over time of WMV and CYSDV in mixed infections in susceptible melon plants, observing greater accumulation of the second, while the viral load of the first is reduced. Transmission by insect vectors was carried out, and the feeding behavior of aphids was analyzed, finding in the case of mixed infections a longer phase associated with WMV acquisition, which could favor its natural dissemination. In experiments with whiteflies in semi-field conditions, better CYSDV transmission was observed towards plants previously infected with WMV, which might favor the prevalence of mixed infections. The analysis of viral suppressors of RNA silencing allowed us to identify an effect caused by the P1 protein of WMV on the activity of P25 of CYSDV. We also confirmed that both proteins can interact, and therefore contribute to specific responses during mixed infections. Finally, NGS of the progeny of CocMoV found insertions and deletions in the polymerase slippage motifs in both P1a and P3, which could lead to the expression of new gene products such as P1aN-SOG and P1aN-ALT. In the case of mixed infections with CYSDV and CocMOV, the relative proportions of P3N-PIPO and P3N-ALT changed compared to simple or mixed infections with WMV.